Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renin granules from rat kidney prepared at 25 degrees C show greater stability at 25 degrees C than at 0 degrees C when incubated in ionic medium. The sum of the renin in the supernatant fluid plus that in the pellet was the same at 25 degrees C as at 0 degrees C, thus ruling out the possibility that the extra release at 0 degrees C merely represented greater stability of free renin at 0 degrees C. In common with other secretory granules, renin granules were most stable at pH 6.0 and were osmotically sensitive. In contrast to neurosecretory and chromaffin granules, renin granules were stabilized by Mg-ATP in ionic medium. This result is similar to studies by others on lysosomes. It is concluded that the renin granules membrane shares many of the properties of other granule membranes. Some of these properties (temperature and pH lability) will have to be considered in the design of future experiments on renin storage and release.
Mol Cell Endocrinol 1976 Oct
PMID:Properties of renin granules isolated from rat kidney. 1 Feb 15

1. The morphology of the juxtaglomerular apparatus, plasma renin activity, plasma renin substrate and renal renin have been studied in rats after maximal stimulation by bilateral adrenalectomy and salt depletion, and also after blocking this stimulation by deoxycorticosterone and salt load. 2. After stimulation the juxtaglomerular apparatus showed a well-developed granular endoplasmic reticulum and a low secretory granule content. Plasma renin activity was markedly elevated and plasma renin substrate was low. After blockade numerous specific granules with crystalline structures were seen and the granular endoplasmic reticulum was less developed. Plasma renin activity was now low and plasma renin substrate elevated. 3. After prior acidification of the kidney extract a significant increase of renal renin was observed in both conditions but was greater in the second group at the time when large numbers of young granules containing crystalline material were seen. 4. Kidney slices from the adrenalectomized salt-depleted rats released more renin than control slices. Vincristine did not affect this release, but inhibited release from slices stimulated by isoprenaline.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Control of renin secretion in vivo and in vitro in rats: arguments in favour of a precursor form of renin and of a role of a microtubular system. 1 63

1. Inactive renin, which can be converted into an active form by acidification to pH 3-3, represents 4-63% of the total renin in rat peripheral plasma. 2. No inactive component could be found in the blood-free venous effluent of the perfused rat kidney before and after stimulation with isoprenaline. 3. This suggests a possible extrarenal source for inactive renin and may explain the presence of this component in anephric patients.
Clin Sci Mol Med 1977 Aug
PMID:Evidence that 'inactive' renin is produced outside the kidney of the rat. 1 91

1. The properties of inactive and active renin in human plasma and amniotic fluid were studied chromatographically. Activation was achieved at pH 3.3 with and without added pepsin. 2. Acid activation of renin was time- and temperature-dependent but was inhibited by dilution of the sample. The dilution effect was corrected by adding pepsin. Such characteristics indicate that activation at low pH is catalysed by intrinsic enzymes. 3. Separation and/or dilution of the activating enzyme during ion-exchange chromatography concealed the eluted position of inactive renin and reduced the amount recovered. Only after full activation of the eluted renin was achieved with added pepsin was a distinct peak of inactive renin exposed. 4. At pH 7.5 inactive renin carried a lower negative charge than the active enzyme. This charge difference was lost after activation. 5. No molecular-weight differences between active, inactive renin or the International Renin Standard were detected by gel filtration. No renin of larger molecular weight was present. 6. These findings will be helpful in purification studies of human inactive renin.
Clin Sci Mol Med 1978 Jul
PMID:The nature of inactive renin in human plasma and amniotic fluid. 2 28

1. Plasma renin activity (PRA) and mean blood pressure were studied in conscious rabbits infused with beta-adrenoreceptor antagonists. 2. Oxprenolol and DL-propranolol each significantly reduced PRA and blood pressure, but prindolol, which had a strong blood pressure-lowering effect, increased PRA. 3. When prindolol was given to animals in which PRA and blood pressure had been reduced by DL-propranolol, PRA returned to control values but blood pressure remained low. Thus the increase in PRA caused by prindolol is not mediated by hypotension. These findings, together with the observation that compound H35/25 reduced PRA without altering blood pressure, suggest that the effects of the beta-adrenoreceptor-blocking drugs on blood pressure are unrelated to their effects on renin release. 4. Studies with D-propranolol and with blocking agents with either beta-1 or beta-2 specificity indicated that the effects of beta-adrenoreceptor blockade on renin are directly dependent upon their action on beta-adrenergic receptors, probably of the beta-2 type.
Clin Sci Mol Med Suppl 1975 Jun
PMID:beta-Adrenergic receptors and renin release: studies with beta-adrenoreceptor-blocking agents in the conscious rabbit. 2 80

1. Angiotensin I-generating activity of rat brain extract was separated into two components by affinity chromatography on a casein-Sepharose gel column. 2. The component without affinity to the gel was identified as true renin on the basis of its sensitivity to anti-renin antibody and the lack of protease activity. 3. The second renin-like component with affinity to the gel was a protease insensitive to the anti-renin antibody. Its renin-like activity examined with sheep substrate was pronounced compared with the rate of angiotensin I generation from the rat substrate. 4. It was concluded that rat brain contains true renin, which can be detected by the use of rat substrate but can be masked when examined with sheep substrate.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. 3 1

1. Active and acid-activable inactive renin were measured in renal venous and arterial plasma of 18 patients with essential hypertension (EHT) and 19 patients with renovascular hypertension (RVHT). In seven patients with EHT and in 11 patients with RVHT measurements were made before and 25-35 min after an intravenous injection of 300 mg of diazoxide. 2. Under basal conditions the renal vein to artery ratios for active and inactive renin in EHT ranged from 0.71 to 1.96 and from 0.68 to 1.44 respectively. In 14 patients with RVHT the renal vein to artery ratio for active renin on the affected side was above the range found in EHT and in six of them the renal vein to artery ratio for inactive renin was also elevated. 3. The diazoxide-induced release of active renin from kidneys, which had a stenotic artery but were not seriously contracted, was associated with a fall of the renal vein to artery ratio for inactive renin to a value below 1.00. 4. The results indicate that changes in the release of active and inactive renin do not always run in parallel. The findings are compatible with the hypothesis that circulating inactive renin can be activated in the kidney.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Renal release of active and inactive renin in essential and renovascular hypertension. 3 2

1. The protease inhibitors Trasylol and soyabean trypsin inhibitor prevented the activation of plasma inactive renin by acid. 2. N-Ethylmaleimide inhibited acid-activation to some extent but o-phenathroline had no effect. 3. Acid-activation of the inactive renin in human plasma is mediated by a serine protease.
Clin Sci Mol Med Suppl 1978 Dec
PMID:An endogenous protease activating plasma inactive renin. 3 3

1. We have found that 'acid'-activation of inactive human plasma renin is a two-phase process. About 30% of activation occurs during dialysis to pH 3.3; the remaining 70% occurs at alkaline pH. 2. The 'alkaline phase' of activation has a pH optimum between 7.5 and 8.4. It is inhibited by unacidified plasma and by soya-bean or lima-bean trypsin inhibitors. 3. 'Cryoactivation' of inactive plasma renin, which occurs at -4 degrees C and alkaline pH, is also inhibited by soya-bean or lima-bean trypsin inhibitors and by the serine protease inhibitors diisopropylphosphorofluoridate and benzamidine. 4. Thus endogenous neutral serine proteases participate in the activation of inactive plasma renin in vitro. Their action is prevented in the circulation by inhibitors which are inactivated by acid or cold.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Activation of inactive plasma renin: evidence that both cryoactivation and acid-activation work by liberating a neutral serine protease from endogenous inhibitors. 3 4

1. The capacity of various tissues of the porcine kidney to convert [1-14C]arachidonic acid into radiolabelled prostaglandins was studied. 2. Only after removal from the cortical matrix, were renal blood vessels able to convert arachidonic acid into prostaglandins (primarily prostacyclin). In contrast, convoluted tubules showed a low capacity to metabolize arachidonic acid. 3. The failure to demonstrate prostaglandin synthesis by renal cortical slices is related to the presence of an inhibitor of cyclo-oxygenase. Thus the addition of renal cortical incubate to isolated vascular tissues and ram seminal vesicles inhibited their ability to synthesize prostaglandins. 4. Slices of renal medulla metabolized arachidonic acid primarily to prostaglandin F2alpha; lesser amounts of prostaglandin E2 and prostacyclin were generated. 5. The large capacity of the renal vasculature to generate prostacyclin is consistent with an important role for this prostaglandin in regulation of renin release and renal haemodynamics.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Endogenous prostaglandin synthesis inhibitor in the renal cortex. Effects on production of prostacyclin by renal blood vessels. 10 75


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